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Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound
DPB162-AE is a valuable tool to study store-operated Ca(2+) entry (SOCE), as this compound was developed as a 2-APB analog that inhibits SOCE more potently and more selectively than 2-APB itself. In addition to this, we showed that, in some conditions, DPB162-AE can deplete the endoplasmic reticulum...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377240/ https://www.ncbi.nlm.nih.gov/pubmed/28393091 http://dx.doi.org/10.1016/j.dib.2017.03.034 |
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author | Bittremieux, Mart Mikoshiba, Katsuhiko Bultynck, Geert |
author_facet | Bittremieux, Mart Mikoshiba, Katsuhiko Bultynck, Geert |
author_sort | Bittremieux, Mart |
collection | PubMed |
description | DPB162-AE is a valuable tool to study store-operated Ca(2+) entry (SOCE), as this compound was developed as a 2-APB analog that inhibits SOCE more potently and more selectively than 2-APB itself. In addition to this, we showed that, in some conditions, DPB162-AE can deplete the endoplasmic reticulum Ca(2+) stores in intact cells, including the cervical carcinoma HeLa cell line and the diffuse large B-cell lymphoma SU-DHL-4 cell line. Here, we present data regarding the toxicity of DPB162-AE in HeLa and SU-DHL-4 cells. For further interpretation of the data presented in this article, please see the research article ‘DPB162-AE, an inhibitor of store-operated Ca(2+) entry, can deplete the endoplasmic reticulum Ca(2+) store’ (M. Bittremieux, J. V. Gerasimenko, M. Schuermans, T. Luyten, E. Stapleton, K.J. Alzayady, et al., 2017) [1]. |
format | Online Article Text |
id | pubmed-5377240 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-53772402017-04-07 Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound Bittremieux, Mart Mikoshiba, Katsuhiko Bultynck, Geert Data Brief Data Article DPB162-AE is a valuable tool to study store-operated Ca(2+) entry (SOCE), as this compound was developed as a 2-APB analog that inhibits SOCE more potently and more selectively than 2-APB itself. In addition to this, we showed that, in some conditions, DPB162-AE can deplete the endoplasmic reticulum Ca(2+) stores in intact cells, including the cervical carcinoma HeLa cell line and the diffuse large B-cell lymphoma SU-DHL-4 cell line. Here, we present data regarding the toxicity of DPB162-AE in HeLa and SU-DHL-4 cells. For further interpretation of the data presented in this article, please see the research article ‘DPB162-AE, an inhibitor of store-operated Ca(2+) entry, can deplete the endoplasmic reticulum Ca(2+) store’ (M. Bittremieux, J. V. Gerasimenko, M. Schuermans, T. Luyten, E. Stapleton, K.J. Alzayady, et al., 2017) [1]. Elsevier 2017-03-23 /pmc/articles/PMC5377240/ /pubmed/28393091 http://dx.doi.org/10.1016/j.dib.2017.03.034 Text en © 2017 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Data Article Bittremieux, Mart Mikoshiba, Katsuhiko Bultynck, Geert Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title | Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title_full | Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title_fullStr | Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title_full_unstemmed | Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title_short | Data on cytotoxicity in HeLa and SU-DHL-4 cells exposed to DPB162-AE compound |
title_sort | data on cytotoxicity in hela and su-dhl-4 cells exposed to dpb162-ae compound |
topic | Data Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5377240/ https://www.ncbi.nlm.nih.gov/pubmed/28393091 http://dx.doi.org/10.1016/j.dib.2017.03.034 |
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